Various theories contend that respiration is tonically stimulated by wakefulness. This wakefulness stimulus is supposedly lost at the transition to nonrapid eye movement sleep, and breathing is then controlled by metabolic systems. In rapid eye movement (REM) sleep, active processes which are specific to that state seem to control breathing, but the details of that control are unknown. This proposal involves analysis of the reality of the wakefulness stimulus and determination of the nature of the tonic and phasic REM sleep influences on breathing. The existence of a wakefulness stimulus will be tested 1) by recording single brain stem respiratory neurons in chronic unanesthetized cats and calculating the relationship between variations in their activity and variations in the power spectrum of the electrocorticogram, 2) by analysis, during the sleep-waking cycle, of the behavior of midbrain reticular neurons which putatively constitute the substrate of the wakefulness stimulus, and 3) by determination of the role of arousal in the response to airway occlusion. Both tonic and phasic REM sleep processes purportedly influence breathing. Phasic influences will be analyzed by calculation of correlation and cross-correlation functions between respiratory neuronal activity and elemental phasic REM events (ponto-geniculo-occipital waves). A possible REM sleep tonic disfacilitation of respiratory motoneurons will be tested by recording and analysis of meduallary respiratory neurons which project to the cord.